Biomedical subjects

A Kiss

Publications and source records attributed to A Kiss.

At least 91 records · Page 5Linked to original sources

PubMed1999

[The hypothalamo-hypophyseal-adrenocortical axis: organization, dynamic aspects and the effect of stress on corticotropin-releasing hormone activity in neurons].

Hypothalamic-hypophyseal-adrenocortical (HPA) axis, often termed stress axis, together with the peripheral sympathetic nervous system and the adrenomedullar hormonal system very sensitively and promptly responds to both external and internal stimuli endangering homeostasis. HPA helps to maintain the physiological equilibrium. The HPA axis forms the first line in the protection of the organism, monitoring the negative factors affecting the stability of the organism by responding by secretion of glucocorticoids. The exaggerated activity of HPA axis is harmful for the organism since it induces a number of disorders including hyperlipidemia, muscle atrophy, hypertension etc., not excluding brain damage. The alterations of the HPA axis lead to hypersecretion of glucocorticoids which may play an important role in the pathology of psychical and neurological diseases. (Tab. 3, Fig. 2, Ref. 31.)

Animals↗

PubMed1998

Induction of p53 and Bax during TGF-beta 1 initiated apoptosis in rat liver epithelial cells.

The relationship between transforming growth factor-beta1 (TGF-beta1) induced growth arrest and apoptosis in rat liver derived epithelial (RLE) cells was analyzed. TGF-beta1 treatment of RLE cells induced both cell cycle arrest and apoptosis. However, pretreatment of the cells with either dexamethasone or cyclohexamide suppressed TGF-beta1 induced apoptosis, without preventing the cell cycle arrest. Both p53 and Bax were subsequently shown to be overexpressed during the TGF-beta1 induced apoptosis. Furthermore, it was revealed that cycloheximide suppressed expression of both p53 and Bax. In contrast, dexamethasone treatment prevented Bax expression alone. Treatment of RLE cells with several growth factors either alone or in combination was ineffective in counteracting TGF-beta1 induced apoptosis. In additon, we show that TGF-alpha also induced both p53 and Bax expressions and augmented TGF-beta-induced apoptosis. Thus, p53 and Bax are likely to be key factors in TGF-beta1 induced apoptosis in RLE cells.

Animals↗

PubMed1998

[The O'Brien filter test in the differential diagnosis of disorders with high-grade thrombocytosis].

In the differential diagnosis of primary and secondary thrombocytosis, platelet function test can be used. We have examined the possible role of O'Brien's filter test in the differentiation of primary and secondary thrombocytosis in 53 patients with myeloproliferative diseases with primary thrombocytosis and in 21 patients with other disorders complicated by secondary thrombocytosis. By using heparin as an anticoagulant, the sensitivity of O'Brien's filter test proved to be 75%, and it's specificity was 85.7%. In blood samples anticoagulated with citrate, the sensitivity was 100% and specificity 83.3%. Based on these studies we suggest the use of O'Brien's filterometer as a screening test in the differential diagnosis in patients with elevated (> 400 x 10(9)/L) platelet count. In case of normal results, the causes of reactive thrombocytosis should be cleared first, while with pathologic results, haematological examination of the patients should be performed.

Chronic Disease↗

PubMed1998

Expression of transforming growth factor-alpha in hepatoblastoma.

BACKGROUND: Transforming growth factor-alpha (TGF-alpha) is a potent stimulator of cell proliferation in the liver and in liver tumors; however, its significance and association with hepatocyte proliferation remains unclear. METHODS: Expression of TGF-alpha and proliferation markers, such as proliferating cell nuclear antigen (PCNA) and cyclin A, were studied and correlated with each other in samples of tumor and surrounding liver tissue taken from nine patients with hepatoblastoma. An avidin-biotin-peroxidase immunohistochemical method was used for detection of TGF-alpha, PCNA, and cyclin A, and in situ hybridization was used to detect TGF-alpha mRNA. RESULTS: Two types of tumor cells of epithelial origin were distinguished based on the expression of TGF-alpha protein and RNA. The more differentiated "fetal" phenotype had a high expression of TGF-alpha and correlated with a low expression of proliferation markers. The less differentiated "embryonal" phenotype had low TGF-alpha expression and high proliferation activity. CONCLUSIONS: The expression of TGF-alpha is associated with a certain morphologic phenotype of tumor cells in hepatoblastoma; higher expression can be detected in more differentiated tumor cells. The negative correlation between the expression of TGF-alpha and proliferation markers suggests that the less differentiated embryonal cells do not depend on growth stimulation provided by TGF-alpha.

Cell Division↗

PubMed1998

Rapid reduction in blood flow to the rat ventral prostate gland after castration: preliminary evidence that androgens influence prostate size by regulating blood flow to the prostate gland and prostatic endothelial cell survival.

BACKGROUND: Androgenic steroids regulate the development and size of the mammalian prostate gland. The mechanism(s) for this growth control might involve a direct effect on prostate cell proliferation and survival as well as more complex effects on the tissue environment supporting nourishment and oxygenation. In this study, we evaluated an animal model of androgen action on the prostate, the rat ventral prostate gland, to determine whether acute androgen withdrawal, by means of castration, might alter the primary blood flow to the prostate gland and for the effects of castration on prostatic endothelial cell viability. METHODS: Groups of rats studied included intact control males, males that had been surgically castrated, or males that received a sham-surgical castration. Relative blood flow (RBF) to the rat ventral prostate glands and rat bladders were measured at 18 and 24 hr after castration or sham castration using a fluorescent microsphere infusion technique. Thin sections from fixed and embedded rat ventral prostate glands obtained from unoperated or 12-hr castrated rats were analyzed by the TUNEL immunostaining technique to microscopically identify and quantify apoptotic epithelial, stromal, and endothelial cells. RESULTS: RBF to the rat ventral prostate was reduced by 38%, at 18 hr after castration when compared with intact or sham-operated rats and by 45% at 24 hr after castration (P=0.038 unoperated/0.025 sham operated). In contrast, RBF to the bladder was not significantly different between any of the groups in the 24-hr castrate experiment. TUNEL staining analysis of ventral prostate tissues obtained from 12-hr castrated rats showed only rare TUNEL-positive epithelial cells similar to the control tissue but significantly increased TUNEL labeling for endothelial and other ventral prostate stromal cells. CONCLUSIONS: Castration resulted in a rapid and significant reduction of blood flow to the mature rat ventral prostate gland that was not seen in the bladder. This reduction precedes the appearance of apoptosis in the epithelial cells of the tissue but more coincided with the appearance of TUNEL-positive prostate vascular endothelial and stromal cells, suggesting that androgens support the survival of cells in the vascular and stromal compartment of the rat prostate as well as in the prostatic epithelium. These preliminary data support the concept that androgen action on the prostate might involve primary regulation of prostate blood flow and prostate vascular cell vitality.

Androgens↗

PubMed1998

Different effects of an oligonucleotide uptake stimulating protein on leukemic cells in their primitive and differentiated state.

The single stranded [3H]oligonucleotide uptake by HL-60 human promyelocyte and K562 human erythroleukemia cells was stimulated 20-45-fold by DUSF (DNA uptake stimulating protein), and this effect was drastically reduced (to 1.6-13x) if the cells were induced to differentiate. The oligonucleotide uptake stimulating effect of DUSF was not altered in HL-60 and K562 cells, if the proliferation of the cells was inhibited by hydroxyurea (HU) treatment. The oligonucleotide uptake by separated granulocytes and mononuclear cells from healthy donors was not stimulated by DUSF, while the uptake of oligonucleotides by myeloid and lymphoid leukemic cells was greatly stimulated (10-15x). The uptake of oligonucleotides by differentiated mononuclear cells of healthy donors could not be stimulated by DUSF, but the oligonucleotide uptake was greatly increased (11x) by DUSF if the cells were subjected to blast transformation.

Biological Transport↗

PubMed1998

Disruption of redox homeostasis in the transforming growth factor-alpha/c-myc transgenic mouse model of accelerated hepatocarcinogenesis.

In previous studies we have demonstrated that transforming growth factor (TGF)-alpha/c-myc double transgenic mice exhibit an enhanced rate of cell proliferation, accumulate extensive DNA damage, and develop multiple liver tumors between 4 and 8 months of age. To clarify the biochemical events that may be responsible for the genotoxic and carcinogenic effects observed in this transgenic model, several parameters of redox homeostasis in the liver were examined prior to development of hepatic tumors. By 2 months of age, production of reactive oxygen species, determined by the peroxidation-sensitive fluorescent dye, 2',7'-dichlorofluorescin diacetate, was significantly elevated in TGF-alpha/c-myc transgenic hepatocytes versus either wild type or c-myc single transgenic cells, and occurred in parallel with an increase in lipid peroxidation. Concomitantly with a rise in oxidant levels, antioxidant defenses were decreased, including total glutathione content and the activity of glutathione peroxidase, whereas thioredoxin reductase activity was not changed. However, hepatic tumors which developed in TGF-alpha/c-myc mice exhibited an increase in thioredoxin reductase activity and a very low activity of glutathione peroxidase. Furthermore, specific deletions were detected in mtDNA as early as 5 weeks of age in the transgenic mice. These data provide experimental evidence that co-expression of TGF-alpha and c-myc transgenes in mouse liver promotes overproduction of reactive oxygen species and thus creates an oxidative stress environment. This phenomenon may account for the massive DNA damage and acceleration of hepatocarcinogenesis observed in the TGF-alpha/c-myc mouse model.

Animals↗

PubMed1998

Reduced activity of hypothalamic corticotropin-releasing hormone neurons in transgenic mice with impaired glucocorticoid receptor function.

Loss of central glucocorticoid receptor (GR) function is thought to be involved in the development of neuroendocrine and psychiatric disorders associated with corticotropin-releasing hormone (CRH) hyperactivity. The possible causal relationship between defective GR function and altered activity of CRH neurons was studied in transgenic mice (TG) expressing antisense RNA against GR. Immunocytochemical studies showed significant reductions in CRH immunoreactive neurons in the paraventricular nucleus (PVN) and in CRH and vasopressin (AVP) stores in the external zone of the median eminence. Concomitantly, stimulus-evoked CRH secretion from mediobasal hypothalami of TG mice in vitro was reduced significantly. However, CRH mRNA levels in the PVN of TG mice were marginally lower than those in wild-type (WT) mice. 125I-CRH binding autoradiography revealed no differences between WT and TG animals in any of the brain regions that were studied. Basal plasma corticosterone (cort) levels and 125I-CRH binding, CRH-R1 mRNA, POMC mRNA, and POMC hnRNA levels in the anterior pituitary gland were similar in WT and TG mice. Intraperitoneal injection of interleukin-1beta (IL-1beta) increased plasma cort levels, CRH mRNA in the PVN, and anterior pituitary POMC hnRNA similarly in WT and TG mice. The injection of saline significantly reduced anterior pituitary CRH-R1 mRNA levels in WT mice, but not in TG mice, whereas IL-1beta produced a decrease in these mRNA levels in both strains. The data show that long-term GR dysfunction can be associated with reduced activity of CRH neurons in the PVN and decreased sensitivity of pituitary CRH-R1 mRNA to stimulus-induced downregulation. Moreover, the hypothalamic changes observed in this model suggest that impaired GR function, at least if present since early embryonic life, does not necessarily result in CRH hyperexpression characteristics of disorders such as major depression.

Animals↗

PubMed1998

Reduced in vitro clot lysis and release of more active platelet PAI-1 in polycythemia vera and essential thrombocythemia.

Because platelets interact with fibrinolysis in a complex manner, it can be expected that with abnormal platelet numbers and quality this interference can be even more profound. The aim of this work was to study the lysis-resistance of platelet-rich clots in diseases with high platelet counts: polycythemia vera (PV), essential thrombocythemia (ET) and to make comparison with polyglobulia (PG). Platelet-rich plasma (PRP) and platelet-poor plasma (PPP) were analyzed by an in vitro clot lysis test. Plasminogen activator inhibitor-1 (PAI-1) activity was measured in plasma and in the supernatants of the washed and gel-filtered platelets after activation by thrombin. The lysis showed decreased speed of PPP-clots in PV and ET. This phenomenon was even more marked in PRP-clots from PV and ET, but further increased lysis resistance after retraction was not observed in PV and ET, most likely due to abnormal platelet functions. Our results suggest that the fibrinolytic activity is reduced in PV and ET, and may play a role both in the increased aptitude for venous thrombosis and in the arterial complications. These are partly caused by higher plasmatic PAI-1 activity as well as by more active platelet PAI-1. The PAI-1 activity was significantly higher in the supernatants of the washed and gel-filtered platelets of PV after activation by thrombin compared with controls. Other factors might have influenced the reduced fibrinolysis.

Adolescent↗

PubMed1998

[From perception to symptom--from symptom to diagnosis. Somatoform disorders as a communication phenomenon between physician and patient].

Patients with somatoform disorders probably constitute the largest diagnostic group in daily medical practice. A major communication problem forms the core of somatoform disorders: patients report about complaints which their physicians do not understand; there is no sufficient biological reason for the patient's symptoms. This article discusses the multifactorial origin of somatoform disorders, consisting of minimal physiological changes, the perception of bodily sensations, and their interpretation as symptoms (non-normal perceptions), as well as ensuing emotional and behavioral consequences. Concerning the communication problem, it is important to realize that patients normally present symptoms, whereas the underlying bodily perceptions and the explanatory models are rarely communicated to the physician. On the physician's side, symptoms presented by patients are subjected to his or her explanatory concepts translating symptoms into indicators of certain diseases. Thus, the information introduced into physician-patient communication by the patient has usually passed several cognitive circuits within the patient or between the patients and other significant conversation partners thus shaping its specific components. It is recommended that physicians try to trace back their patients' symptoms to bodily sensations and explanatory models in order to base their diagnostic and therapeutic reasoning on the same kind of information. Empirical evidence is presented to support the inter-dependence of the components of the model, on both the patient's and the physician's side. Therapeutic interventions based upon the model are presented.

Awareness↗

PubMed1998

Dexamethasone inhibits the proliferation of hepatocytes and oval cells but not bile duct cells in rat liver.

Recent advances have implicated the importance of tumor necrosis factor (TNF) and interleukin 6 (IL-6) in the regulation of liver growth. Therefore, we studied how dexamethasone, a well-known inhibitor of these cytokines, influences the proliferation of different hepatic cell populations. As we expected, dexamethasone pretreatment suppressed the expression of both TNF and IL-6 after partial hepatectomy and significantly reduced the proliferative response of the hepatocytes. Furthermore, the proliferative response of hepatocytes could be rescued by IL-6 administration. Dexamethasone also severely diminished the induction and expansion of oval cells induced by the 2-acetylaminofluorene/partial hepatectomy (AAF/PH) protocol but did not have any effect on the proliferation of the bile duct cells stimulated by bile duct ligation. The differential inhibition of these two morphologically very similar cell types may be used to characterize divergent regulatory mechanisms responsible for the proliferative response of oval cells and adult bile epithelial cells.

Animals↗

PubMed1998

Plaque excision and dermal graft in the surgical treatment of plastic induration of the penis (Peyronie's disease).

Excision of the fibrous plaque from the full thickness of the tunica albuginea of the corpora cavernosa of the penis was performed in 16 patients with Peyronie's disease in the course of seven years. The resulting gap was covered with a dermal flap. The dorsal vascular and neural bundles were separated from the tunica albuginea together with Buck's fascia. This method caused only very slight damages in the circulation and innervation of the penis. The patients were satisfied with the straightness of their penis. The method has the following advantages: it may be applied even in case of extensive, cartilaginous, calcified plaques; the hourglass deformation of the penis may be corrected; it does not result in the shortening of the penis; the complete excised plaque may be examined histologically.

Adult↗

PubMed1998

Leiomyoma of the female urethra.

Leiomyoma of the female urethra is an uncommon but benign condition. The authors report two additional cases of successfully operated neoplasms. The difficulties of the diagnosis, differential diagnosis, the surgical treatment and the complications are discussed.

Adult↗

PubMed1998

Mean corpuscular volume is not a reliable marker of red cell age in case of anisocytosis.

The present study was designed to determine the effect of anisocytosis on the association of MCV values with HbA1c and reticulocyte counts as markers of red cell age. Normo-, micro- and macrocytic samples, fractionated by counterflow centrifugal elutriation were studied. The previously described correlation between MCV and HbA1c was only observed in normal samples and in the middle fractions of samples with anisocytosis. At both extremes of the elutriation profile, curves for HbA1c content and reticulocyte count levelled out. Furthermore, in fractions containing the largest red cells of the microcytic series and the smallest red cells of normo- and macrocytic samples, reticulocyte count decreased while HbA1c content increased with increasing MCV. From these data it is concluded that MCV is not an absolute determinant of red cell age in case of anisocytosis.

Erythrocyte Aging↗

PubMed1998

Atresia of the appendix.

A 4-day-old black male underwent laparotomy for intestinal obstruction. At surgery, multiple jejunal atresias (type IV) of the jejunum were detected. As an incidental finding, atresia of the appendix was also present. The jejunal atresia was repaired, and resection of the tip of the cecal pole and atretic appendix was performed. Gross and histological examination confirmed the presence of a type IV atresia of the jejunum and a cordlike (type II) atresia of the appendix with inflammatory changes in the tip of the appendix. The boy made an uneventful recovery. Examination of all organ systems did not show any associated findings, and the family history was unremarkable. To our best knowledge, this case represents the first case of atresia of the appendix described in the literature.

Appendix↗

PubMed1998

Stress and colchicine do not induce the release of galanin from the external zone of the median eminence.

The aim of the present study was to verify the hypothesis that stress exposure modifies the content and release of galanin in the hypothalamic paraventricular nucleus and the median eminence. Colchicine and immobilization served as stress stimuli, and the changes in galanin immunoreactivity were compared with those in corticotropin-releasing hormone and vasopressin. In control animals, a limited number of galanin perikarya were identified in the paraventricular nucleus. The high dose (75 microg) of colchicine enhanced galanin in both parvicellular and magnocellular subdivisions, as analysed 72 h later. In the median eminence, galanin accumulated only in the external zone. High-dose colchicine did not affect galanin, while corticotropin-releasing hormone and vasopressin were depleted from the median eminence. Immobilization (120 min) neither alone nor in combination with colchicine influenced galanin immunoreactivity in the external zone. The low dose of colchicine induced an unexpected accumulation of galanin in the internal zone of the median eminence, which was further increased by subsequent immobilization. In the external zone, low-dose colchicine induced a complete disappearance of vasopressin, substantial depletion of corticotropin-releasing hormone and no changes in galanin immunoreactivity. The present studies demonstrate that galanin in the external zone of the median eminence is not influenced by colchicine or by immobilization stress.

Animals↗

PubMed1998

Brain angiotensin II modulates sympathoadrenal and hypothalamic pituitary adrenocortical activation during stress.

Angiotensin II (Ang II) type-1 (AT1) receptors are present in areas of the brain controlling autonomic nervous activity and the hypothalamic-pituitary-adrenal (HPA) axis, including CRH cells in the hypothalamic paraventricular nucleus (PVN). To determine whether brain AT1 receptors are involved in the activation of the HPA axis and sympathetic system during stress, we studied the effects of acute immobilization stress on plasma catecholamines, ACTH and corticosterone, and mRNA levels of CRH and CRH receptors (CRH-R) in the PVN in rats under central AT1 receptor blockade by the selective antagonist, Losartan. While basal levels of epinephrine, norepinephrine and dopamine in plasma were unaffected 30 min after i.c.v. injection of Losartan (10 microg), the increases after 5 and 20 min stress were blunted in Losartan treated rats (P < 0.05 for norepinephrine, and P < 0.01 for epinephrine and dopamine, vs controls). Basal or stress-stimulated plasma ACTH and corticosterone levels were unaffected by i.c.v. Losartan treatment. Using in situ hybridization studies, basal levels of CRH mRNA and CRH-R mRNA in the PVN were unchanged after i.c.v. Losartan. While Losartan had no effect on the increases in CRH-R mRNA levels 2 or 3 h after 1 h immobilization, it prevented the increases in CRH mRNA. The blunted plasma catecholamine responses after central AT1 receptor blockade indicate that endogenous Ang II in the brain is required for sympathoadrenal activation during immobilization stress. While Ang II appears not to be involved in the acute secretory response of the HPA axis, it may play a role in regulating CRH expression in the PVN.

Adrenal Cortex↗

PubMed1998

Raised levels of exhaled carbon monoxide are associated with an increased expression of heme oxygenase-1 in airway macrophages in asthma: a new marker of oxidative stress.

BACKGROUND: Chronic inflammatory diseases are associated with an increased production of oxidants. Induction of a stress protein, heme oxygenase (HO) HO-1, is a cytoprotective mechanism against oxidative cellular injury. HO-1 catabolises heme to bilirubin, free iron, and carbon monoxide (CO). METHODS: Exhaled CO and sputum bilirubin levels were measured and HO-1 protein expression in airway macrophages was determined by Western blotting in asthmatic patients as levels of oxidants are raised in asthma and may induce HO-1. RESULTS: Exhaled CO was significantly increased in 37 non-steroid treated asthmatic patients compared with 37 healthy subjects (5.8 (95% CI 5.20 to 6.39) ppm vs 2.9 (2.51 to 3.28) ppm; p < 0.0001) but was similar to normal in 25 patients who received corticosteroids (3.3 (95% CI 2.92 to 3.67) ppm; p > 0.05). In non-treated asthmatic patients more HO-1 protein was expressed in airway macrophages than in normal subjects. Bilirubin levels in induced sputum were also higher than in normal subjects. Inhalation of hemin, a substrate for HO, significantly increased exhaled CO from 3.8 (95% CI 2.80 to 4.87) ppm to 6.7 (95% CI 4.95 to 8.38 CI) ppm (p < 0.05) with a concomitant decrease in exhaled nitric oxide levels, suggesting an interaction between the two systems. CONCLUSIONS: Increased exhaled CO levels and HO-1 expression may reflect induction of HO-1 which may be inhibited by steroids. Measurement of exhaled CO, an index of HO activity in non-smoking subjects, may therefore be clinically useful in the detection and management of asthma and possibly other chronic inflammatory lung disorders.

Adult↗